I. Field of the Invention
This invention relates generally to cardiac rhythm management devices, and more particularly to an apparatus for determining the efficacy of pacing/defibrillation therapy chronically using a catheter mounted strain gauge placed on or in the heart.
II. Discussion of the Prior Art
It is now recognized that patients suffering from congestive heart failure (CHF) can be benefited using a cardiac rhythm management device (CRMD) to deliver cardiac stimulating pulses to the heart in timed relation to the heart's own cardiac cycle. For example, the Baumann U.S. Pat. No. 5,800,471 describes a cardiac rhythm management device especially designed for treating CHF. The device described in the Baumann '471 patent incorporates a programmed microcontroller that is operative to adjust the pacing mode and/or AV delay of the CRMD so as to achieve optimum hemodynamic performance. One measure of hemodynamic performance is the heart's contractility, which is a measure of the strength of the pumping action of the heart.
It is known in the art to provide a pressure sensor in one or more cardiac chambers to monitor pressures in the atrial and/or ventricular chambers of the heart in assessing contractility. Electrogram signals have also been signal processed and used to infer changes in contractility. More recently, a chronically implantable intracardiac acceleration sensor has been developed by Sorin Biomedica, of Saluggia, Italy, that allows quantitation of cardiac acceleration. The sensor is a micromass, uniaxial acceleration sensor located in the pacing tip of a standard unipolar pacing lead, which is adapted to be implanted in the apex of the right ventricle. Because the sensor capsule is non-deformable, the accelerometer is thought to be relatively insensitive to the potential effects of tissue encapsulation. During isometric contraction of the heart, the myocardium generates vibrations, the audible component of which comprises the first heart sound, that can be detected by intracardiac accelerometry. Because this occurs during isovolumic contraction, the effect is independent of after-load and may reflect myocardial contractility. Because the left ventricular musculature comprises most of the myocardium, the peak-to-peak amplitude of the peak endocardial acceleration has been hypothesized to reflect left ventricular contractility. Further information concerning the use of an acceleration sensor for measuring peak endocardial acceleration can be found in a paper by Occhetta et al. entitled “Experience With a New Myocardial Acceleration Sensor During Dobutamine Infusion and Exercise Test”, published in the European Journal of Cardiac Pacing Electrophysiology, Vol. 5, pp. 204-209 (1995).
Generally speaking, the availability of miniature accelerometers available to measure fractional “g” range changes is low and this is based on the fact that accelerometer sensitivity is inversely proportional to the mass of the accelerometer. Thus, a need exists for an improved sensor that can be chronically placed in or on the heart for measuring contractility changes occasioned by the administration of pacing or drug therapy to patients suffering from CHF. The present invention fulfills such a need.